Preparticipation Screening and Prevention of Sudden Death

For more than 20 years systematic preparticipation screening, based on 12-lead ECG in addition to history and physical examination, has been the practice in Italy [6, 41]. This screening strategy has proven to be effective in the identification of athletes with previously undiagnosed hypertrophic cardiomyopathy, due to the high sensitivity (up to

95%) of 12-lead ECG for suspicion/detection of this condition in otherwise asymptomatic athletes. Moreover, during long-term follow-up no deaths were recorded among these disqualified athletes with hypertrophic cardiomyopathy, suggesting that restriction from competition may reduce the risk of sudden death [6].

Despite the high prevalence of ECG abnormalities, such as T-wave inversion in right precordial leads and ventricular arrhythmias with a left bundle branch block morphology at preparticipation evaluation, the majority of sudden death victims from ARVC/D had not been identified at preparticipation screening, thus explaining why this condition was previously reported to be the leading cause of sudden death in Italian athletes [6,12]. The most plausible explanation is that, unlike HCM, ARVC/D is a condition that was discovered only recently (approximately two decades ago) and was either underdiag-nosed or regarded with skepticism by cardiologists. Recently, Corrado et al. reported the results of a timetrend analysis of the changes in incidence rates and causes of sudden cardiovascular death in young athletes age 12-35 years in the Veneto region of Italy between 1979 and 2004, after the introduction of systematic preparticipation screening [42]. Over the same time interval, they performed a parallel study which examined trends in cardiovascular causes of disqualification from competitive sports in 42,386 athletes undergoing preparticipation screening at the Center for Sports Medicine in Padua. Fifty-five sudden cardiovascular deaths occurred in screened athletes (1.9 deaths/100,000 person-years) and 265 deaths in unscreened nonathletes (0.79 deaths/100,000 person-years). The annual incidence of sudden cardiovascular death in athletes decreased by approximately 90%, from 3.6/100,000 person-years in 1979-1980 to 0.4/100,000 person-years in 2001-2004, whereas the incidence of sudden death among the unscreened nonathletic population did not change significantly over that time. The decline in the death rate started after mandatory screening was initiated and persisted to the late screening period. Compared with the pre-screening period (1979-1981), the relative risk of sudden cardiovascular death was 44% lower in the early screening period (1982-1992) and 79% lower in the late screening period (1993-2004). Most of the reduced death rate was due to fewer cases of sudden death from cardiomyopathies, mostly from ARVC/D. Time-trend analysis showed that the incidence of sudden death from this latter condition fell by 84% over the 24-year span (Fig. 22.3). This decline of mortality from cardiomyopathies paralleled the concomitant increase in the number of athletes with cardiomyopathies (both

Trends for sudden death from ARVC/D from 1979-2004: The effect of screening on mortality

Early-screening (1982-1992) Sudden death per 100,000 athlete-years

Fig. 22.3 • Average annual incidence rates of sudden death from ARVC/D among young competitive athletes of the Veneto Region of Italy, before and after implementation of systematic preparticipation screening. Death rates from ARVC/D declined from 0.90 per 100,000 person-years in the 1979-1981 prescreening period to 0.15 per 100,000 in the 1993-2004 late-screening-period (RR=0.16, 95% CI 0.031.41; p for trend=0.02)

hypertrophic cardiomyopathy and ARVC/D) who were identified and disqualified from competitive sports over the screening periods at the Center for Sports Medicine in Padua. Screening athletes for cardiomyopathies is a life-saving strategy and 12-lead ECG is a sensitive and powerful tool for identification, risk stratification and management of athletes affected by hypertrophic cardiomyopathy and ARVC/D [41,42].

Was this article helpful?

0 0

Post a comment